Abstract

目的:探讨幽门螺杆(Helicobaaterpyloti,丘pylon)感染与胃黏膜细胞叉头蛋白3(forkhead3,Foxp3)、肿瘤生长因子-131(tumorgrowthfactor-131,TGF一131)、白介素-10(interleukin-10,IL-10)表达的关系.方法:按照病理检查结果将100例胃镜检查患者分为实验组(胃癌)30例和对照组(慢性浅表性胃窦炎、慢性萎缩性胃炎、胃溃疡、十二指肠溃疡)70例,比较两组患者Hpylori感染情况及胃黏膜细胞Foxp3、TGF-β1及IL-10的表达.结果:本组100例患者HPylori阳性72例(72.00%),实验组感染率为63.33%,对照组感染率为75.71%,总感染率为72.00%;Foxp3mRNA在实验组和对照组阳性表达率比较(73.33%VS54.29%),差异无统计学意义(P〈0.05);Foxp3mRNA在H.pylori感染阳性组阳性表达率与Hpylori感染阴性组阳性表达率比较(68.06%VS39.29%),差异具有统计学意义(P〈0.05);TGF-β1mRNA在实验组和对照组阳性表达率比较(73.33%vs62.86%),差异无统计学意义(p〉0.05);TGF.BlmRNA在H.pylori感染阳性组阳性表达率与Hpylori感染阴性组阳性表达率比较,(75.00%VS 42.86%),差异具有统计学意义(P〈0.05);两组患者Hpylori阳性IL-10蛋白含量均显著高于Hpylori阴性(3.58pg/mL4±0.65pg/mLvs0.58pg/mL±0.03pg/mL.2.84pg/mL4±0.89pg/mLVS0.97pg/mL4±0.22pg/mL),差异具有统计学意义(P〈0.01).结论:Hpylori感染后,可诱导Treg细胞Foxp3的高表达以及TGF-β1、IL-10表达上调,抑制机体胃黏膜局部免疫功能,为Hpylori的持续性感染提供了微环境.

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